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相关概念视频

Role of ER in the Secretory Pathway01:17

Role of ER in the Secretory Pathway

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Eukaryotic cells have a special pathway that enables communication between various intracellular membrane-bound compartments and also with the extracellular environment. This pathway is termed as the secretory pathway.
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...
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Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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Tail-anchoring of Proteins in the ER Membrane01:45

Tail-anchoring of Proteins in the ER Membrane

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Tail-anchored, or TA, proteins are estimated to make up to 3-5% of membrane proteins found in the eukaryotic cell. Such proteins have a single transmembrane domain located approximately 30 amino acid residues upstream from the C-terminal end. As a result, the signal recognition particle (SRP) cannot guide a TA protein to the ER membrane for cotranslational insertion. Hence, they are integrated into the ER membrane post-translationally using their C-terminal end as the anchor. TA proteins...
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ER Retrieval Pathway01:45

ER Retrieval Pathway

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In the secretory pathway, vesicles transport proteins from one cellular compartment to another in forward transport to deliver the protein to its correct location. Occasionally, misfolded proteins and incorrect proteins escape their original compartments, and a retrieval pathway is used to return the escaped proteins to their original compartment.
The ER uses many checkpoints to prevent the entry of incorrectly folded or a resident protein as cargo onto a transport vesicle. These mechanisms...
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Regulation of the Unfolded Protein Response01:31

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
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在内分泌疗法耐药乳腺癌中,胺诱导的内分泌网膜压力是可向的脆弱性

Purab Pal1, Shweta Chitkara2, Godwin K Sarpey1

  • 1Department of Physiology and Biophysics, University of Illinois Chicago, IL, USA.

bioRxiv : the preprint server for biology
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概括
此摘要是机器生成的。

乳腺癌的内分泌疗法耐药性包括胺的减少和对胺诱导的细胞死亡的敏感性增加. 陶胺通过PERK激活内质网膜应激 (EnRS) 途径,导致抵抗性细胞的细胞死亡,特别是通过TRAM1相互作用.

关键词:
陶化物与胺相互作用的蛋白质内分泌疗法耐药性细胞内膜网应力乳腺癌的发明美国一个TRAM1

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科学领域:

  • 癌症学
  • 分子生物学
  • 细胞生物学

背景情况:

  • 内分泌疗法 (ET) 对激素受体阳性乳腺癌是有效的,但由于治疗耐药性和患者复发而面临挑战.
  • 抗ET乳腺癌细胞表现出胺代谢的改变,显示胺水平的降低和对胺诱导的细胞死亡的敏感性增加.

研究的目的:

  • 研究胺在耐ET乳腺癌细胞中诱导细胞死亡的机制.
  • 确定涉及ET耐药性中胺介导细胞死亡途径的特定蛋白质.

主要方法:

  • 在胺治疗后对抗ET细胞的转录重编程的分析.
  • 评估内质网膜应激 (EnRS) 和PERK通路在胺诱导的细胞死亡中的作用.
  • 使用可光激活的胺探针来识别胺相互作用蛋白 (CIP).
  • 在ET抗性模型和患者数据中研究TRAM1的功能.

主要成果:

  • 在耐ET细胞中诱导明显的转录重编程,上调EnRS通路.
  • 胺诱导的EnRS依赖于PERK通路,并在多个ET耐药模型中调解细胞死亡.
  • TRAM1被确定为ET耐药细胞中的关键胺相互作用蛋白 (CIP),与较低的无复发存活率和侵袭性乳腺癌表型相关.
  • TRAM1的破坏模仿了胺在ET抵抗中的作用,突出显示了它在胺诱导的细胞死亡中的作用.

结论:

  • 与ET敏感细胞相比,耐ET乳腺癌细胞对PERK介导的EnRS更敏感.
  • 胺利用这种敏感性与TRAM1等CIP相互作用,激活PERK,并在ET耐药模型中诱导细胞死亡.
  • 向胺-TRAM1-PERK轴为克服乳腺癌中ET抗性的潜在治疗策略.